In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilatio
n associated with increases in the acute ventilatory responses to hypoxia (
AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes
the converse of these effects, three 8-h protocols were compared in 14 sub
jects: 1) poikilocapnic hyperoxia, With end-tidal Po-2 (PETO2) = 300 Torr a
nd end-tidal P-co2 (PETCO2) uncontrolled; 2) isocapnic hyperoxia, with PETO
2 = 300 Torr and PETCO2 maintained at the subject's normal air-breathing le
vel; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were d
etermined before and 0.5 h after each exposure. During isocapnic hyperoxia,
after an initial increase, ventilation progressively declined (P < 0.01, A
NOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventila
tion at fixed PETCO2 decreased (P < 0.05); and 3) air-breathing PETCO2 incr
eased (P < 0.05); but 4) no significant changes in AHCVR or intercept were
demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to
those found with 8 h of hypoxia, indicating that there may be some "acclim
atization to hypoxia" at normal sea-level values of Po-2.